Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: HUMANGGP:001400 (PRP)
 1,320 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet-poor plasmas (PPPs) from 52 out of 71 patients affected by different diseases and selected for increased amounts of circulating platelet aggregates, incubated at 37 degrees C for 30 min with control platelet-rich plasma (PRP; cross-matching test) induced the formation of platelet aggregates, stimulated the production of malondialdehyde and enhanced ADP-induced aggregation. 31 control PPPs were consistently negative at cross-matching test. Gel chromatography of plasmas on agarose 4% allowed the identification of four different fractions (A, B, C, D) provided with aggregating activity. Fraction A eluted at the void volume was to be identified with the von Willebrand factor, whereas B, C and D fractions, eluted at the same elution volumes as activated factor X were mainly composed of factor X (fraction B) and activated factor X (fractions C and D). Thrombin activity was absent in all the fractions provided with aggregating activity. Also, from control PPPs negative at cross-matching tests, the same fractions could be obtained, although of 5--10 times lower aggregating potency, thus explaining the negative cross-matching tests. These findings stress the role of some extraplatelet factors related to hypercoagulability in platelet hyperaggregability.
 ...
PMID:Increased platelet aggregation due to plasma-aggregating activity. Identification of the responsible factors. 676 58

Addition of Ristocetin to formalin-fixed platelets suspended in diluted PPP induces a marked increase in turbidity which is not caused by platelet shape change but by the formation of microaggregates. If diluted PPP of patients with severe von Willebrand's disease is used, only an initial increase in turbidity and no further decrease is observed without any form variation of the platelets but again with formation of many microaggregates. In normal PRP diluted with buffered EDTA, ADP induces an increase in turbidity without further changes in optical density. Simultaneously platelets immediately change their shape with formation of pseudopodia and sphering but at the same time also microaggregates appear. Shape change and microaggregate formation can also be observed after the addition of Collagen to undiluted PRP which is followed by the formation of large aggregates and a decrease in optical density. Increase in optical density in undiluted PRP is not a specific indicator of platelet shape changes. Microaggregates can alone or partially be responsible for these changes. For the evaluation of platelet shape changes but also for the estimation of microaggregate formation microscopic methods are preferred.
 ...
PMID:Optical density variations and microscopic observations in the evaluation of platelet shape change and microaggregate formation. 678 Oct 96

The dependence of ADP- and epinephrine-induced platelet aggregation and secretion on extracellular divalent cations was examined by quantitating these responses in citrate-, heparin-, and hirudin-anticoagulated platelet-rich plasma. ADP-induced 14C-5HT secretion in heparin-PRP and hirudin-PRP was generally decreased, relative to that in citrate-PRP, without corresponding reductions in aggregation, whereas in response to epinephrine, both aggregation and secretion were decreased in heparin-PRP, and abolished in hirudin-PRP. In heparin-PRP, but not in hirudin-PRP, the degree to which these responses were altered was highly variable among normal subjects, and was dependent on the anticoagulant concentration. Addition of citrate restored the extent of ADP-induced secretion and of epinephrine-induced aggregation and secretion in heparin-PRP to that observed in citrate-PRP, and increased the extent of ADP-induced secretion in hirudin-PRP. Addition of EDTA or EGTA, however, had no effect of ADP-induced secretion in heparin-PRP. These results suggest that ADP-induced aggregation and secretion, as well as responses to ADP vs. epinephrine, have different dependencies on extracellular or surface-bound divalent cations. The variable responses observed in heparin-PRP may reflect direct interactions of heparin with platelets, and this variability may account for the conflicting results of previous studies.
 ...
PMID:Dependence of human platelet functional responses on divalent cations: aggregation and secretion in heparin- and hirudin-anticoagulated platelet-rich plasma and the effects of chelating agents. 678 96

Infusion of PGI2 at a dose of 5 or 10 ng/kg/min during 72 hours into patients with peripheral vascular disease was followed by increased susceptibility of platelets to proaggregatory action of ADP and collagen but not that of arachidonate. The above effects were observed 24 hours after termination of infusion of PGI2. A tendency to an increased formation of TXA2 in PRP aggregated by arachidonate was also noticed. Infusion of PGI2 at a dose of 2 mg/kg/min during 72 hours into the patients caused the decreased platelet aggregability to ADP and arachidonate but not to collagen, and a decreased tendency to production of TXA2 in PRP aggregated by arachidonate. The existence of a "rebound effect" in platelets after a long term PGI2 therapy is suggested.
 ...
PMID:Increased platelet activity after termination of prostacyclin infusion into man. 680 7

Addition of arachidonic acid to human platelet rich plasma caused a reversible aggregation, which was greatly decreased after aspirin ingestion. ADP induced a greater aggregation, which was only slightly decreased after aspirin ingestion. When PRP was incubated with arachidonic acid for 2 or 6 min before the addition of ADP, the ADP-induced aggregation was greatly decreased. This decrease was not changed by aspirin ingestion. The present study indicates that arachidonic acid is metabolized in human platelets not only to aggregatory compounds but also to anti-aggregatory compound(s). The formation of the latter compound is not inhibited by aspirin.
 ...
PMID:The effect of arachidonic acid on the aggregability of human platelet rich plasma. 680 91

A new method for the separation from plasma and washing of human platelets is described. The use of prostacyclin (PGI2) throughout the procedure prevents the activation of platelets. The method allows a 60-70% yield of platelets from PRP. The platelet sensitivity to ADP, collagen, adrenaline, arachidonic acid and thrombin is the same as in PRP. The platelet suspension is stable for long periods and the reactivity to aggregating agents remains unchanged for periods greater than 48 h when platelets are stored at 4 degrees C.
 ...
PMID:The use of prostacyclin in the separation from plasma and washing of human platelets. 681 68

Understanding the nature and regulation of very early events in the platelet activation sequence is an important goal. A general approach based on quenched-flow principles has therefore been developed. Platelet reactions are initiated by mixing inducing agent with whole blood, PRP, or washed platelets and pumping the mixture through narrow-bore tubing with quenching (stopping the reaction) at the outlet. Reaction times less than 1 sec are feasible. The quenched-flow system has been combined with a continuous-flow modification of resistive-particle counters to follow aggregation kinetics of "single" particles. Aggregation at 37 degrees is extremely rapid: after a lag period of about 1 sec, between 20% and 50% of platelets then aggregate per second (10 micro M ADP). Although the kinetics are second order, data can be expressed as the percent of "single" platelets aggregating per second and treated as pseudo-first order. This enables derivation of apparent maximal velocities of aggregation and inducer activation constants, for characterizing platelet reactivity.
 ...
PMID:Rapid reactions of platelets studied by a quenched-flow approach: aggregation kinetics. 681 89

Recent investigations have shown that human and canine platelets possess a new pathway for securing irreversible platelet aggregation independent of ADP secretion and prostaglandin synthesis. Platelet activating factor (PAF) is a potent aggregating agent for rabbit platelets and is also reputed to stimulate the cells by a completely independent pathway. Since the newly recognized mechanism in human and dog cells, termed membrane modulation, might be mediated by PAF, we evaluated the influence of this agent on human cells. Results of that study demonstrated that PAF did not activate platelets through an independent pathway and was not involved in the mechanism of membrane modulation. In the present investigation we have examined the possibility that PAF might act on human platelets through the mechanism of membrane modulation. Human platelets were made refractory to amounts of PAF routinely causing irreversible aggregation by prolonged incubation of C-PRP at 37 degrees C, by exposure to PGI2 or aspirin, or by aggregation-disaggregation of control or aspirin treated cells. Epinephrine at concentrations which did not cause aggregation turned on the mechanism of membrane modulation in refractory platelets and restored their sensitivity to PAF. Thus, PAF does not appear to activate human platelets through a unique, independent pathway. Rather, it usually causes irreversible aggregation of human cells through the mechanisms of ADP secretion and thromboxane synthesis or, as shown in this study, can be dependent on membrane modulation.
 ...
PMID:Platelet activating factor (PAF) causes human platelet aggregation through the mechanism of membrane modulation. 681 43

We examined the extent of lytic and sublytic platelet injury after exposure of platelets to shear stress and the role in shear-induced PAG of ADP liberated from platelets as a result of shear-induced platelet dense body release and/or platelet damage. Platelets in C-PRP or TAS were subjected to well-defined, laminar shear stress in a rotational viscometer, and PAG (loss of single, nonaggregated platelets), 14C-serotonin release, and loss from platelets of LDH and 51Cr were determined. Increased PAG with increasing shear stresses was associated with progressive loss of LDH and 51Cr. Loss of 51Cr was consistently in excess of that of LDH, indicating sublytic platelet injury, which was confirmed by electron microscopy. At the lowest shear stress used (50 dynes/cm2), PAG in C-PRP was observed in the absence of detectable loss of 51Cr or LDH. When platelets in TAS were sheared in the presence of CP/CPK, an enzyme system capable of removing extracellular ADP, PAG was only partially (approximately 40%) inhibited. However, when platelets were preincubated with CP/CPK and ATP (to saturate platelet ADP receptors), shear-induced PAG was almost completely suppressed. Similar results were obtained with PAG induced by collagen in the aggregometer. The findings indicate that (1) shear-induced PAG in this system may occur without measurable lytic or sublytic platelet damage and (2) ADP liberated from platelets as a result of shear-induced release or damage may represent the major if not sole mediator of shear-induced PAG.
 ...
PMID:Role of cytoplasmic and releasable ADP in platelet aggregation induced by laminar shear stress. 683 26

Pyridoxal 5'-phosphate (PALP) inhibited ADP, thrombin, adrenaline, PAF and AA induced aggregation and 14C-5HT release. Thromboxane B2 (TxB2) generation induced by all the above agents except AA was also inhibited indicating that PALP may be inhibiting AA release via phospholipase A2 activation rather than AA metabolism. PALP inhibited ristocetin induced aggregation in PRP and agglutination in formaldehyde-treated washed platelets (FWP). Inhibition of ADP, adrenaline, PAF and AA-induced aggregation and 14C-5HT release by PALP was found in resuspended platelets pretreated with PALP and sodium borohydride suggesting that inhibition was mediated by Schiff base formation with platelet surface amino groups. Irreversible fixation of PALP to the platelet membrane by borohydride reduction also inhibited thrombin induced 14C-5HT release and TxB2 generation but no thrombin induced primary aggregation or ristocetin induced agglutination in FWP. This suggests that PALP may interact with specific glycoproteins on the platelet membrane involved in ADP, adrenaline and PAF induced primary aggregation and that PALP could be inhibiting ristocetin induced agglutination by direct interaction with ristocetin or F VIII RCoF.
 ...
PMID:Effect of pyridoxal 5'-phosphate (PALP) on human platelet aggregation, dense granule release and thromboxane B2 generation--role of Schiff base formation. 689 Nov 7


<< Previous 1 2 3 4 5 6 7 8 9 10